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|Title:||Metallothionein 2A expression is associated with cell proliferation in breast cancer||Authors:||Jin, R.
Thameem, Dheen S.
|Keywords:||Science & Technology
Life Sciences & Biomedicine
|Issue Date:||1-Jan-2002||Publisher:||OXFORD UNIV PRESS||Citation:||Jin, R., Thameem, Dheen S., Duan, W., Bay, B.-H., Chow, V.T.-K., Tan, P.-H. (2002-01-01). Metallothionein 2A expression is associated with cell proliferation in breast cancer. Carcinogenesis 23 (1) : 81-86. ScholarBank@NUS Repository.||Abstract:||Metallothioneins (MTs) belong to a family of cysteinerich, metal-binding intracellular proteins, which have been linked with cell proliferation. In this study, expression levels of the 8 known MT-1 and MT-2 functional isoforms in human invasive ductal breast cancer specimens were determined by RT-PCR. The expression profiles of the MT protein and MT-2A mRNA were further evaluated in 79 cases of human invasive ductal breast carcinoma by immunohistochemistry and in situ hybridization, and correlated with cancer cell proliferation (determined by ki-67 nuclear antigen immunolabeling). MT-1A, MT-1E, MT-1F, MT-1G, MT-1H, MT-1X and MT-2A but not MT-1B, were detected in breast cancer tissue samples. The MT-2A mRNA transcript was the highest among all the isoforms detected. A positive correlation was observed between MT-2A mRNA and MT protein expression with Ki-67 labeling (P = 0.0003 and P < 0.0001, respectively) but not with apoptosis (P = 0.1244 and P = 0.8189, respectively). Co-localization of the MT protein and Ki-67 nuclear antigen in breast cancer cells was demonstrated by double immunofluorescence staining. There was also significantly higher MT protein and MT-2A mRNA expression in histological grade 3 tumors than in histological grade 1 and 2 tumors. The finding that MT 2A appears to be the main isoform associated with cell proliferation in invasive ductal breast cancer tissues, may have therapeutic implications.||Source Title:||Carcinogenesis||URI:||http://scholarbank.nus.edu.sg/handle/10635/33868||ISSN:||01433334
|Appears in Collections:||Staff Publications|
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